Food allergies are a growing health concern with dramatic increase in the last two decades. More than 12 million US Americans suffer from food allergies. The incidence of food allergy is highest in young and decreases with age.
Allergic responses caused by food allergy can range from mild responses, such as dermatitis, gastrointestinal and respiratory distress, to severe reactions, such as anaphylaxis, including biphasic anaphylaxis and vasodilation. Anaphylaxis is a life threatening systemic condition, causing a constriction of the trachea, preventing breathing, and anaphylactic shock. Peanuts and tree nuts account for the majority of the life-threatening and fatal reactions.
Food-induced allergic reactions result from immunological pathways that include activation of effector cells through food specific IgE antibodies, cell-mediated (non-IgE-mediated) reactions resulting in subacute or chronic inflammation, and the combination of these pathways. Several studies investigating pathogenesis of food allergy point to a functional role for regulatory T lymphocytes (Treg) in the development of normal tolerance to food allergens and the spontaneous resolution of milk allergy (Karlsson M R, Rugtveit J, Brandtzaeg P. J Exp Med 199(12), 1679-1688 (2004), Sletten G B, Halvorsen R, Egaas E, Halstensen T S. International archives of allergy and immunology 142(3), 190-198 (2007)). Oral immune tolerance is indeed dependent on the induction of allergen-specific Treg cells that block the generation of allergen-specific IgE. In patients with food allergy, oral immunotherapy has been reported to be associated with changes in various immune parameters, including a boosting of levels of IgG4 and IgA, reduction in basophil and mast cell reactivity; and changes in Treg cell or T effector cell numbers. Development of milk-specific Tregs in milk allergic subjects ultimately led to tolerance, indicating that Tregs may be a driving force in outgrowth of milk allergy (Shreffler, et al. J. Allergy Clin. Immunol., 123 (2009), pp. 43-52).
There is no treatment commercially available to treat a food allergy. The current standard of care is strict avoidance of the offending allergens and immediate access to rescue medications, such as epinephrine and antihistamines. Indeed, the great majority of allergic patients are treated by symptomatic medication using drugs that, for example, prevent the degranulation of mast cells, exhibit general anti-inflammatory activity and/or reverse bronchoconstriction or vasodilatation. However, symptomatic medication fails to target the mechanisms underlying allergic disease, and often has only short activity.
There is a need for an effective long-term treatment and protection against food allergies.